In conclusion, Vimentin plays an important role in hypoxia induced VM formation of RCC cells and targeted Vimentin might be beneficial for RCC therapy.
Compared with adjacent normal tissues, the mRNA and protein expression levels of LOXL2, FAK, Src, MMP‑9, N‑cadherin and vimentin and the levels of FAK and Src phosphorylation were increased, while the mRNA and protein expression levels of E‑cadherin were decreased in RCC tissues.
Therefore, the purpose of this work was to (1) evaluate the expression of EMT markers: ZEB2, vimentin, N-cadherin, TWIST, PTEN, survivin, E-cadherin, Ki-67 and GLUT-1, (2) assess mutation status of two genes: PIK3CA and KRAS, and (3) investigate the potential relationships between the studied biomarkers and clinicopathological factors in clear-cell renal cell carcinoma (ccRCC).
After collecting tissues from the chest wall tumor via needle biopsy, the pathological examination was combined with positive immunoreaction of CD10, epithelial membrane antigen, and vimentin, and the patient was diagnosed with metastatic CCRCC in the chest wall deposits.
In the present study, it was demonstrated that in the RCC cell lines 786‑O and Caki‑1 treated with VPA, the neural (N)‑cadherin, vimentin and SMAD4 protein and mRNA levels were decreased, accompanied with an increase in expression of epithelial (E)‑cadherin.
We investigated the usefulness of napsin A and paired box gene 8 (PAX-8) with previously studied markers epithelial membrane antigen (EMA), carcinoembryonic antigen (CEA), vimentin and cluster of differentiation marker 10 (CD10) in differentiating CCRCC from hidradenoma.
Furthermore, the chromatin immunoprecipitation assay indicated that pCREB (Ser133) had a direct interaction with the fibronectin promoter, however, pCREB (Ser133) did not target the vimentin promoter in RCC.
Specimens from these patients were stained by HE and immunohistochemistry for the detection of WT1, vimentin, S-100 protein, CK7, P504s, CD10 and renal cell carcinoma marker (RCC).
Multivariate analyses revealed that CXCR4 and VIM up-regulation represents an independent prognostic marker for poor cancer specific survival in patients with renal cell carcinoma.
Most importantly, a 15-fold inactivation of GSK-3β activity, 3-fold decrease of E-cadherin, and 2-fold increase of vimentin were observed in human RCC tumor tissues.
Genome-wide gene expression analysis (miR‑138 transfectants and RCC clinical specimens) and TargetScan database studies showed that vimentin (VIM) is a promising candidate target gene of miR‑138.
Among others, vimentin, heat shock protein 27 (Hsp27), annexin IV and serum amyloid alpha-1 (SAA-1) have been identified as reliable markers of RCC that are potentially useful in the clinical setting.
Panels of immunohistochemical stains are proposed for different settings, including renal cell carcinoma (RCC) marker, CD10, and vimentin to suggest renal origin of a metastatic tumor, and markers to aid in subclassification of RCC, including parvalbumin and c-kit for chromophobe RCC, and cytokeratin 7 and alpha-methyl-acyl-CoA racemase for papillary RCC.
Consistent with our cDNA microarray data, chromophobe RCCs and oncocytomas exhibited similar expression profiles: 8 of 8 examples of each subtype were immunohistochemically positive for beta defensin-1 and parvalbumin and negative forvimentin (sensitivity 100%, specificity 100%); 4 of 7 papillary RCCs were positive for beta defensin-1, parvalbumin, and vimentin (sensitivity 57%, specificity 97%); and 22 of 23 conventional RCCs were negative for beta defensin-1, parvalbumin, or both markers (sensitivity 96%, specificity 96%) as well as positive for vimentin (sensitivity 83%).